在非恶性结肠表皮质中Di(2-乙烯基) 甲的细胞效应涉及氧化应激
Zachary S Bomstein1, Kimberly F Allred1, Clinton D Allred1
1Department of Nutrition, University of North Carolina at Greensboro, 319 College Ave., Greensboro, NC 27412, USA.
International journal of molecular sciences
|December 11, 2025
概括
甲基二甲基甲酸盐 (DEHP) 在非恶性结肠细胞中引起氧化应激和亡,部分是通过阿里碳水化合物受体 (AhR) 引起的. 这种甲酸盐暴露会影响细胞水平的胃肠道毒性.
科学领域:
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
- 胃肠病学 胃肠病学
背景情况:
- 人类暴露于2-乙基) 甲酸盐 (DEHP) 主要是通过摄入食物.
- 之前关于DEHP胃肠道毒性的研究使用了恶性细胞系,限制了对健康上皮质的影响的理解.
- 在非恶性肠道上皮质中DEHP的分子信号传递仍然不太清楚.
研究的目的:
- 为了研究DEHP在体外对非恶性结肠上皮细胞的影响.
- 描述DEHP引起的结肠中毒性的细胞机制.
- 探索阿里尔碳化合物受体 (AhR) 在DEHP毒性的作用.
主要方法:
- 使用未经转换的年轻成年老鼠结肠细胞 (YAMC) 细胞系.
- 72小时暴露于DEHP的YAMC,并评估了细胞数量,增殖,亡和反应性氧物种 (ROS) 生产.
- 采用CRISPR技术来删除YAMC中的阿里尔碳化合物受体 (AhR),用于机械研究.
- 研究了与氧化应激相关的基因表达,包括BAX,NRF2,GCLC,HO-1和CHOP.
主要成果:
- 暴露于DEHP显著降低了YAMC细胞数量和增殖.
- 短期的DEHP暴露增加了细胞亡,BAX表达,ROS产生和与氧化压力相关的基因表达.
- 抗氧化剂预处理减轻了DEHP诱导的亡,这表明氧化应激和亡之间存在联系.
- DEHP的亡和亲氧化作用部分由阿里尔碳化合物受体 (AhR) 介导.
结论:
- 在非恶性结肠细胞中,DEHP诱导的毒性是由ROS诱导的氧化应激介导的,导致亡.
- 亚利碳水化合物受体 (AhR) 在调解DEHP的毒性作用方面起着部分作用.
- 需要进一步的研究来阐明将ROS与亡联系在一起的特定机制以及对DEHP响应的AhR信号的动态.
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